This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Michalopoulos, G. K. Articles by Jirtle, R. L. Search for Related Content PubMed Articles by Michalopoulos, G. K. Articles by Jirtle, R. L. Social Bookmarking                         What's this?

Mechanisms of Rodent Liver Carcinogenesis

Departments of Pathology and Radiology Duke University Medical Center Durham, North Carolina

Peter M. Eckl

Departments of Pathology and Radiology Duke University Medical Center Durham, North Carolina

Jennifer L. Cruise

Departments of Pathology and Radiology Duke University Medical Center Durham, North Carolina

Deborra L. Novicki

Department of Pathology University of North Carolina Chapel Hill, North Carolina

Randy L. Jirtle

Departments of Pathology and Radiology Duke University Medical Center Durham, North Carolina

Stimulation of DNA synthesis by peroxisonte proliferators, including DEHP, should be viewed differently from the stimulation of DNA synthesis by xenobiotic chemicals which stimulate restorative hyperplasia after hepatic necrosis induced by the toxicity of the chemical. The emerging picture of the control mechanisms for hepatocyte proliferation suggests that rather few and distinct factors are involved. The stimulation of DNA synthesis by peroxisome proliferators should be examined in the context of the effects of these factors. Comparisons with other xenobiotics show that induction of DNA synthesis at rates comparable to those of peroxisome proliferators is not sufficient to explain the rates of carcinogenicity associated with peroxisonie proliferators. These considerations lead to the conclusion that although DNA synthesis enhances the incidence of neoplasia, it should not be viewed as a complete carcinogen, nor should it be considered as resulting in initiation at rates that can explain the carcinogenic potency of compounds such as peroxisome proliferators.

Key Words: hepatocarcinogenesis • hepatocyte proliferation • hepatopoietins • norepinephrine • peroxisome proliferators.

Toxicology and Industrial Health, Vol. 3, No. 2, 119-128 (1987)
DOI: 10.1177/074823378700300209


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?